OBJECTIVES: This study investigate the clinical and imaging features of Ewing sarcoma (ES) of the jaw. METHODS: Eight cases of pathologically diagnosed ES of the jaw from January 2010 to June 2022 were included in the study. Clinical and radiological features were retrospectively analyzed. RESULTS: Among the eight cases, the mean age at onset was 29.4 years, and the male to female ratio was 7∶1. The predilecting site was the posterior part of mandible, accounting for 75% of the cases. The lesions often exhibited early numbness of the lower lip and lymphadenopathy. The main radiographic manifestation of mandibular lesions was ill-defined radiolucency, mixed with fibrous or brush-like tumor matrix, and soft tissue mass. The maxillary ES lesions mainly presented as lytic bone destruction accompanied by adjacent soft tissue mass. Periosteal ossification was rarely seen. CONCLUSIONS The clinical and imaging characteristics of ES in the jaw are helpful for its diagnosis.
Male ; Humans ; Female ; Sarcoma, Ewing/pathology* ; Retrospective Studies ; Radiography ; Mandible/pathology* ; Lip ; Bone Neoplasms

Objective:To investigate the impact of cleavage factor Im25(CFIm25)on VSMCs-specific knockdown in the context of hyperlipidemia.Methods:Mice models were constructed with specific knockout of CFIm25 in VSMCs(CFIm25f/+ TaglnCre)and control mice(TaglnCre).The mice were fed a normal diet or high-fat diet(HFD)for 18 weeks and their body weight changes were monitored.ELISA was used to measure serum total cholesterol(TC), triacylglycerol(TG), high-density lipoprotein(HDL-C)and low-density lipoprotein(LDL-C)levels.The extent of aortic lipid deposition in mice was assessed by oil red O staining.Results:During the feeding of a high-fat diet, CFIm25f/+ TaglnCre mice showed a significant increase in body weight compared to the control group[Male(1.01±0.06)g and(0.87±0.31)g, t=7.53, P<0.05; Female: (0.64±0.02)g and(0.35±0.04)g, t=9.68, P<0.05].After 18 weeks of high-fat diet feeding, CFIm25f/+ TaglnCre mice had significantly higher levels of TC[(6.80±0.35)mmol/L and(3.76±0.87)mmol/L, t=5.63, P=0.004], TG[(0.97±0.21)mmol/L and(0.42±0.10)mmol/L, t=4.08, P=0.015], and LDL-C[(5.20±0.30)mmol/L and(2.00±0.98)mmol/L, t=5.40, P=0.006]compared to the TaglnCre group.Specifically, TC levels increased by 80.72%, TG increased by 132.79%, and LDL-C increased by 160.32%.There was a significant increase in aorta lipid deposition and atherosclerotic plaque area in CFIm25f/+ TaglnCre mice( P<0.05). Conclusions:The research indicated that VSMCs-specific CFIm25 knockdown in mice further worsened hyperlipidemia and atherosclerotic lesions.

OBJECTIVE： To systematically evaluate the efficacy and safety of TCM compound preparation for tonifying kidney and activating blood circulation， and to provide evidence-based reference for rational drug use in the clinic. METHODS： By retrieving Cochrane library， PubMed， Embase， CBM， CNKI， VIP and Wanfang database， randomized controlled trials （RCTs） about TCM compound preparation for tonifying kidney and activating blood circulation （trial group） versus calcium or non-calcium agents （control group） in the treatment of postmenopausal osteoporosis were included. After literature screening， data extraction and quality evaluation with bias risk evaluation tool and Jadad scale of Cochrane system evaluator manual 5.1.0， Meta-analysis was conducted by using Stata 12.0 software， and trial sequential analysis （TSA） was conducted by using TSA 0.9 software. RESULTS： Totally 18 RCTs were included， involving 1 408 patients. The results of Meta-analysis showed that total response rate [RR＝1.35，95％CI（1.17，1.54），P＜0.000 1] and bone density[SMD＝0.24，95％CI（0.16，0.32），P＜0.000 1] of trial group were significantly higher than those of control group； blood calcium [SMD＝－0.05，95％CI（－0.09，0.00）， P＝0.033] of trial group was significantly lower than that of control group. There was no statistical significance in the levels of urine creatinine [SMD＝－1.60，95％CI（－5.94，2.74），P＝0.470]， urinary calcium/urine creatinine ratio [SMD＝－0.05，95％CI（－0.14，0.04），P＝0.295]， urinary hydroxyproline/urine creatinine ratio [SMD＝－0.16，95％CI（－1.04，0.72），P＝0.726]， ALT [SMD＝0.51，95％CI（－3.26，4.28），P＝0.790]， AST [SMD＝0.23，95％CI（－5.22，4.77），P＝0.929]， serum alkaline phosphatase [SMD＝－0.22，95％CI（－0.68，0.25），P＝0.361]， serum phosphate [SMD＝－0.02，95％CI（－0.11，0.07），P＝0.639]， urea nitrogen [SMD＝－0.19，95％CI（－0.70，0.31），P＝0.453]， estradiol [SMD＝0.62，95％CI（－0.28，1.52），P＝0.177]， IL-6 [SMD＝－1.78，95％CI（－4.86，1.30），P＝0.258] or VAS [SMD＝0.55，95％CI（－1.03，2.13），P＝0.496] between 2 groups. No server ADR was found in 2 groups. TSA showed that there were extract evidences for total response rate of TCM compound preparation in the treatment postmenopausal osteoporosis. CONCLUSIONS： TCM compound preparation for tonifying kidney and activating blood circulation shows significant therapeutic efficacy for postmenopausal osteoporosis， and can improve serum calcium and bone density with good safety.

Objective To investigate the protective role of carbon monoxide releasing molecule-2 (CORM-2) in post-resuscitation myocardial dysfunction (PRMD) in rat models of cardiopulmonary resuscitation (CPR).Methods Cardiopulmonary resuscitation model was established after cardiac arrest induced by ventricular fibrillation.Male healthy Sprague-Dawley (SD) rats were randomly (random number) divided into 4 groups according to random number table:control group,CORM-2 group,inactive CORM-2 (iCORM-2) group and Sham group,in which the equal volume (1 mL) of 0.2％ DMSO,50 μmol/kg CORM-2,50 μmol/kg iCORM-2 and 0.2％ DMSO were respectively administered into the rats of these groups after resuscitation.The ejection fraction (EF) of left ventricle and myocardial performance index (MPI) were measured to detect the myocardial function by echocardiography at 12 hours after resuscitation.Mitochondrial respiration was assessed with Clark oxygen electrode at the same time.Western blot was used to determine the ratio of mitochondrial cytochrome c (cyt c) to cytoplasmic cyt c as well as caspase-3 level.Multiple comparisons were made by analysis of variance.Results Compared with the control group,higher EF and MPI,higher state Ⅲ respiration rate and respiratory control rate (RCR) of mitochondria,and decreased ratio of mitochondrial cytc/cytoplasmic cyt c and lower caspase-3 level were observed in the CORM-2 group (P ＜ 0.05).However,there were no significant differences in above biomarkers found between iCORM-2 group and control group (P ＞ 0.05).Conclusions The CO released from CORM-2 might improve mitochondrial respiration and PRMD by inhibition of myocardial apoptosis via a mitochondrial pathway.

Objective To investigate the resuscitation outcome after a short period of mild hypothermia in porcine model of prolonged ventricular fibrillation (VF).Methods Fourteen male healthy domestic swine weighting 34 to 36 kg were used.VF was induced electrically and maintained untreated for 11 mins,followed by manual cardiopulmonary resuscitation (CPR) procedure.Two investigators initiated chest compression and bag-valve mask ventilation in pattern of 2 min rotation.A biphasic wave of 120 J electric defibrillation (ED) was attempted 6 mins after CPR.If there was no return of spontaneous circulation (ROSC),CPR was restored and ED was delivered when necessarily.Resuscitation was considered unsuccessful if absence of ROSC for 12 mins.However,if ROSC occurred,animals were randomly (random number) diveded into normothermia (NT) group and hypothermia treatment (CH) group.Animals in CH group were immediately cooled by using intravenous infusion of ice-cold saline and surface cooling.Core temperature was reduced to 32-34 degrees centigrade within 120 mins and maintained at this level for 2 h.Active rewarming was completed within 2 h until baseline body temperature was reached.Data of hemodynamic variables,blood-gas analysis and blood lactate before VF of two groups were recorded.Meawhile,cardiac output (CO),heart rate and Tc after ROSC were recorded.Neurological defect scores (NDS) were evaluated every 24 h until 96 h after ROSC.Variables were compared using either Fisher test or repeated measures analysis of variance,followed by Bonferroni for multiple comparisons.A two-sided P value ＜0.05 was regarded statistically significant.Results There was no significant difference in body weight,mean arterial pressure,CO,pH,pressure of end-tidal carbon dioxide (ETCO2) and lactate between groups before VF.In the period of CPR,there were also no significant difference in total resuscitation time,first shock success rate,ROSC rate,shock ROSC rate,total number of shock and doses of epinephrine.However,animals in CH group survived longer time than that in NT groups [(96.00 ± 0.00) hvs.(49.71 ±43.65) h,P=0.031].Meanwhile,the survival rate of 96 h was significantly higher in CH than that in NT (P ＜ 0.05).For neurological function,there was a obviously better NDS in CH group than that in NT group within ROSC 96 h (P ＜ 0.05).Conclusion Even a short duration of 2 hour mild hypothermia could improve resuscitation outcome in porcine model of 11 minute VF.

Objective: Numerous studies have shown that bone marrow-derived mesenchymal stem cells (MSCs) enhance neurological recovery after cerebral ischemia. However, the mechanisms are still not clear. The present study aimed to investigate the beneficial effects of MSCs on global cerebral ischemia induced by cardiac arrest (CA) and the underlying mechanisms. Methods: Rats subjected to asphyxial CA were injected intravenously with MSCs (5×106 ) at 2 hours after resuscitation. Whole brain histopathologic damage scores (HDS) were assessed by histopathology at 3 and 7 days after resuscitation. The distribution of donor MSCs in the brain was evaluated. The expression of tumor necrosis factor-α-induced protein 6 (TSG-6) and pro-inflammatory cytokines in cerebral cortex was assayed. After intravenous infusion of TSG-6 siRNA-MSCs, HDS and pro-inflammatory cytokines were reevaluated at 7 days after resuscitation. Results: Intravenously administered MSCs significantly reduced whole brain HDS after global cerebral ischemia. Immunofluorescence microscopy revealed that donor MSCs were primarily found in cerebral cortex and expressed TSG-6. MSCs treatment significantly increased the expression of TSG-6 and reduced the expression of pro-inflammatory cytokines in cerebral cortex. In addition, intravenous infusion of TSG-6 siRNA-MSCs failed to attenuate brain inflammation. Conclusion: Systemically administered MSCs reduced inflammatory damage to brain in rats with global cerebral ischemia via secretion of TSG-6.
Heart Arrest ; Mesenchymal Stromal Cells

Objective To explore the therapeutic potential and mechanism of stem cells mobilized by granulocyte colony-stimulating factor (G-CSF) and AMD3100 to repair global cerebral ischemia injuries in a rat model of cardiac arrest (CA) and cardiopulmonary resuscitation (CPR).Methods Cardiac arrest was induced by asphyxia.Fifty-six SD rats were randomly assigned into four groups:G-CSF group,G-CSF + AMD3100 group,CPR control group and sham operated group.The animals were sacrificed at 3d and 6d after CPR respectively.The neurological status and morphological changes of damaged cerebrum,the apoptosis of nerve cells and vascular endothelial growth factor (VEGF) expressed in brain tissue and capillary density in hippocampus and temporal lobe cortex were measured and analyzed by means of neurological deficit score (NDS),adhesive tape removal test (TRT),ELISA,MRI and immunofluorescence.Results NDS in G-CSF + AMD3100 group (61.4 ± 10.7) was significantly higher than that in CPR control group (49.9 ± 10.4) at 3 d after CPR (P ＜0.05).And less time consumption for TRT found in G-CSF + AMD3100 group (85.5 ±28.9) s rather than was in CPR control group (148.1 ± 23.8) s and G-CSF group (118.5 ± 30.4) s (P ＜ 0.05).The severity of cerebral injury assessed by MRI was significantly milder at both 3 d and 6 d in the two stem cell mobilization groups.The apoptosis rate of nerve cells in G-CSF + AMD3100 group (0.23 ± 0.06) was significantly lower than that in G-CSF group (0.34 ±0.08) at 3 d after CPR,and that in both stem cell mobilization groups was lower than that in CPR control group (0.44 ± 0.09) (P ＜ 0.05).At 3 d and 6 d after CPR,the levels of VEGF in brain tissue were (106.2 ±23.3) pg/mL and (79.9 ± 18.4) pg/mL in G-CSF + AMD3100 group,and were (50.6 ± 13.7) pg/mL and (73.9 ± 16.6) pg/mL in G-CSF group,which were both significantly higher than that in CPR control group (23.1 ± 10.2) pg/mL and (36.2 ± 12.8) pg/mL (P ＜0.05).At 3 d after CPR,the cerebral capillary density (351.8 ±67.9) branches in every high power field (A/HPF) was significantly higher in G-CSF + AMD3100 group than that (301.4 ± 77.3) A/HPF in G-CSF group and (250.4 ± 48.0) A/HPF in CPR control group (P ＜ 0.05).The cerebral capillary density in G-CSF group elevated to (348.4 ±76.7) A/HPF at 6 d after CPR which was significantly higher than that at 3 d (P ＜0.05),and there was no difference between that at 3 d and 6 d in G-CSF + AMD3100 group.Conclusions The mobilization stem cells improve the impaired neurological function.The increased expression of VEGF in brain tissue,the neo-vascularization promoted by the mobilized stem cells and the inhibition of nerve cell apoptosis may be associated with the protective effects of the stem cell mobilization.

Objective To compare the difference in cardiac injuries between asphyxia and ventricular fibrillation modes in different periods after cardiac arrest (CA).Methods The model was established in Cardiopulmonary Resuscitation Lab,Sun Yat-sen University.A total of 35 male SD rats were used to produce the asphyxia or ventricular fibrillation (VF) cardiac arrest models randomly.Both of the two modes were induced 8 minutes cardiac arrest.The myocardial HE stains,mitochondrial respiratory control ratio (RCR),and echocardiography were observed at 4 h,24 h and 72 h after ROSC (restoration of spontaneous circulation).The results were expressed as (-x ± s),t test was performed to compare between two groups,and one way analysis of variance was used to compare multiple groups.P ＜ 0.05 was considered as significant difference.Results HE stains showed damages were more serious in the VF mode than in asphyxia mode at 4 h,and both of them had a disorderly-arranged myocardium at 72 h.RCR in VF mode became worse at 4 h,and RCR resumed at 24 h in both modes without significant difference compared with the sham operated rats.The echocardiography showed VF mode had a lower left ventricular ejection fraction (LVEF) than asphyxia mode at 4 h (29.68％ vs.42.16％,P =0.03),and there was no difference in LVEF between VF mode and the sham operated rats at 24 h,however no difference in LVEF between the asphyxia and sham operated rats at 72 h.Both of them had a thicker left ventricular anterior wall than the sham operated rats at 72 h (2.41 mm vs.1.72 mm,P=0.013; 2.61 mmvs.1.72 mm,P=0.007),and there was no significant difference between them.Conclusions The ventricular fibrillation mode has a more severe injuries in early period,but it recovers sooner than asphyxia one.Both of two groups get compensatory left ventricular hypertrophy in later period of ROSC.

Objective To investigate the effects of mitochondrial division inhibitor 1 (mdivi-1) in rats after cardiopulmonary resuscitation (CPR) and its mechanism.Methods Fifty Sprague-Dawley (SD) rats were randomly (random number table) divided into sham group (n =8),cardiac arrest (CA) model group (n =14),dimethyl sulfoxide post-treatment control group (DMSO group,n =14),and mdivi-1 post-treatment group (mdivi-1 group,n =14).Asphyxial CA was reproduced in animals,and they were resuscitated by CPR.In the mdivi-1 group or DMSO group,the animals were given mdivi-1 (1.2 mg/kg) or DMSO (0.1％) intravenously after restoration of spontaneous circulation (ROSC).The neurological functions were assessed using neurological deficit score (NDS) determined at 24,48 and 72 hours after CPR.The brain tissues were harvested at 72 hours after CPR.The histopathologic changes were assessed by hematoxylin and eosin (HE) staining,and the normal neuron was counted.The neuronal apoptosis was assessed with terminal dexynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining,and the expressions of cytochrome C (Cyt-C) protein in mitochondria and cytoplasm from hippocampus were determined by Western Blot.Results NDS in all experiment groups was gradually increased after CPR,and they were significantly lower than thoseo.f the sham group at 24,48,and 72 hours (51.5±3.7 vs.80.0±0.0,59.3±3.6 vs.80.0±0.0,66.7±2.6 vs.80.0±0.0,all P ＜ 0.05).The number of normal pyramidal neurons in the hippocampal CA1 region was markedly reduced (cells/HP:4.4± 1.1 vs.23.1 ± 4.0,P ＜ 0,05),the apoptotic index was significantly increased [(86.9 ± 6.9)％ vs.(3.4 ± 0.8)％,P ＜ 0.05],the expressions of Cyt-C in mitochondria were significantly decreased (A value:0.46±0.18 vs.1.00±0.00,P ＜ 0.05),and the expressions of Cyt-C in cytoplasm were significantly up-regulated (A value:6.65±0.21 vs.1.00±0.00,P ＜ 0.05).Compared with the CA group,NDS at 24 hours and 48 hours in mdivi-1 group was slightly increased (55.2 ± 3.3 vs.51.5 ± 3.7,64.7 ± 2.4 vs.59.3 ± 3.6,both P ＞ 0.05),and it was significantly increased at 72 hours (74.5±2.3 vs.66.7 ± 2.6,P ＜ 0.05),the number of normal pyramidal neurons in the hippocampal CA1 region was markedly increased (cells/HP:16.2±2.4 vs.4.4± 1.1,P ＜ 0.05),the apoptotic index was dramatically reduced [(42.3 ± 3.9)％ vs.(86.9 ± 6.9)％,P ＜ 0.05],the expressions of Cyt-C in mitochondria were significantly increased (A value:0.83 ± 0.22 vs.0.46 ± 0.18,P ＜ 0.05),and the expressions of Cyt-C in cytoplasm were significantly decreased (A value:3.84±0.47 vs.6.65±0.21,P ＜ 0.05).There was no statistically significant difference in above indexes between CA group and DMSO group.Conclusion By inhibiting mitochondrial Cyt-C apoptotic pathway to reduce neuronal apoptosis in rats after CA-CPR,mdivi-1 can improve brain function after CPR.

Objective To study the establishment of rat model of asphyxia-cardiac arrest and efficacy of CPR in order to find the length of optimum time of asphyxia to cause injury.Methods One hundred and twenty-six male Sprague-Dawley rats were randomly (random number) divided into sham operation group and experimental groups.Cardiac arrest was induced by asphyxiation after intravenous injection of vecuronium bromide.The experimental groups were assigned into AP4 (four-minute asphyxia period),AP6 and AP8 subgroups in accordance with different lengths of time of asphyxia subjected to.In these groups,CPR,including pre-cordial compression and synchronized mechanical ventilation,was initiated 4,6 and 8 min after asphyxia-induced cardiac arrest,respectively.The successful ratio of resuscitation and hemodynamic variables were recorded.Brain water content,neural deficit scores (NDS),imaging changes on MR,pathological changes of brain tissue and neuronal apoptosis were evaluated at 1 d,3 d and 7 days after ROSC.All the data were analyzed by single-factor analysis of variance or Chi-square test.P ＜ 0.05 was considered statistically significant.Result The lowest NDS occurred at 1 d after ROSC,brain water content and imaging changes on MR were most obvious at 3 d after ROSC,while pathological changes of brain tissue and neuronal apoptosis increased and reached the peak at 7d after ROSC.The survival rates after 24 hours of AP4,AP6 and AP8 groups were 85％,75％ and 45％,respectively.The rate of ROSC and survival rate of AP8 group were significantly lower than those of other groups (P ＜0.01).The longer time of asphyxia the severer pathological changes of brain tissue,brain edema,neural deficit,and magnetic resonance imaging changes in all experimental groups.As compared to other groups,the brain damage index of AP8 group was most serious,while that of AP6 group was moderate.Conclusions The rat model following asphyxia-induced cardiac arrest and cardiopulmonary resuscitation was established successfully.From the evidence of survival rate and damage grade of brain tissue,asphyxia for 6 min may be the rational length of ischemic time in this model.